scholarly journals Calcium-Calmodulin-dependent Protein Kinase II and Protein Kinase C-mediated Phosphorylation and Activation ofd-myo-Inositol 1,4,5-Trisphosphate 3-Kinase B in Astrocytes

1999 ◽  
Vol 274 (21) ◽  
pp. 14734-14742 ◽  
Author(s):  
David Communi ◽  
Valérie Dewaste ◽  
Christophe Erneux
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Dependent Protein Kinase ◽  
Calcium Calmodulin Dependent ◽  
Kinase C ◽  
Inositol 1,4,5 Trisphosphate ◽  
Protein Kinase Ii ◽  
Dependent Protein

scholarly journals Neuronal Protection and Preservation of Calcium/Calmodulin-Dependent Protein Kinase II and Protein Kinase C Activity by Dextrorphan Treatment in Global Ischemia

1993 ◽  
Vol 13 (4) ◽  
pp. 550-557 ◽  
Author(s):  
Jaroslaw Aronowski ◽  
M. Neal Waxham ◽  
James C. Grotta
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Neuronal Morphology ◽  
Global Ischemia ◽  
Specific Substrate ◽  
Dependent Protein Kinase ◽  
Calcium Calmodulin Dependent ◽  
Kinase C ◽  
Protein Kinase Ii ◽  
Dependent Protein

This study analyzed the ability of the N-methyl-d-aspartate receptor antagonist dextrorphan (DX) to prevent neuronal degeneration (analyzed by light microscopy), calmodulin (CaM) redistribution (analyzed by immunocytochemistry) and changes in activity of two major Ca2+-dependent protein kinases—calcium/calmodulin-dependent protein kinase II (CaM-KII) and protein kinase C (PKC) (analyzed by specific substrate phosphorylation) after 20 min of global ischemia (four-vessel occlusion model) in rats. DX treatment before and after ischemia significantly protected hippocampal and cortical neurons from neurodegeneration whereas DX posttreatment alone did not have any effect on preservation of neuronal morphology as compared with placebo treatment analyzed 72 h after 20 min of ischemia. Similarly to histological changes, DX exhibited protection against redistribution of CaM observed after ischemia. These changes were detected both in hippocampus as well as in cerebral cortex. Finally, DX administered before ligation of the carotid arteries reduced loss in both CaM-KII and PKC activity evoked by ischemia.

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